https://scholars.lib.ntu.edu.tw/handle/123456789/468545
Title: | Vascular endothelial function and circulating endothelial progenitor cells in patients with cardiac syndrome X | Authors: | Huang P.-H. Chen Y.-H. YUH-LIEN CHEN Wu T.-C. Chen J.-W. Lin S.-J. |
Issue Date: | 2007 | Journal Volume: | 93 | Journal Issue: | 9 | Start page/Pages: | 1064-1070 | Source: | Heart | Abstract: | Background: Endothelial dysfunction and microvascular abnormalities have been reported in patients with cardiac syndrome X (CSX), but the underlying mechanisms are unclear. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow-derived endothelial progenitor cells (EPCs). Aim: To test the hypothesis that the biology of altered EPCs might contribute to the pathophysiology of CSX. Methods: 34 subjects (mean (SD) age: 62 (7) years) were enrolled in the study, including 12 patients with CSX, 12 stable subjects with coronary artery disease (CAD) and 10 healthy controls. The number and adhesive function of EPCs were measured in peripheral-blood samples from these study participants. Results: The baseline characteristics in patients with CSX and CAD were enhanced Framingham risk scores, more hypertension and lower high-density lipoproteins than the controls. Patients with CSX and CAD had significantly decreased endothelium-dependent flow-mediated vasodilation (FMD) compared with normal controls (normal controls vs CSX vs CAD: 10.6% (3.5%) vs 6.1% (1.8%) vs 4.1% (1.9%), p<0.001), but the difference was not found in endothelium-independent nitroglycerine-mediated vasodilation (p = 0.159). Reduced numbers of colony-forming units (CFU) of EPCs were noted in patients with CSX and CAD (normal vs CSX vs CAD: 41 (9) vs 30 (7) vs 14 (7) CFU/well, p<0.001). Levels of EPCs were shown to be associated with FMD (r = 0.557, p = 0.001) and high-density lipoprotein (r = 0.339, p = 0.049). Also, attenuated fibronectin adhesion function of EPCs was found in patients with CSX and CAD compared with normal subjects (104 (12) vs 80 (20) vs 65 (13)/well, p<0.001). Conclusions: This study clearly showed for the first time that compared with normal subjects, patients with CSX have decreased levels and adhesive function of circulating EPCs. These findings may explain the underlying mechanisms which contribute to the endothelial dysfunction and microvascular abnormalities observed in patients with CSX. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-34548145571&doi=10.1136%2fhrt.2006.107763&partnerID=40&md5=61dc59f46bcf086a33321484dab0d345 https://scholars.lib.ntu.edu.tw/handle/123456789/468545 |
ISSN: | 1355-6037 | DOI: | 10.1136/hrt.2006.107763 | SDG/Keyword: | angiotensin receptor antagonist; dipeptidyl carboxypeptidase inhibitor; glyceryl trinitrate; high density lipoprotein cholesterol; hydroxymethylglutaryl coenzyme A reductase inhibitor; adult; aged; article; blood sampling; cardiac syndrome x; cell function; cell regeneration; clinical article; controlled study; coronary artery disease; endothelial dysfunction; female; heart disease; human; hypertension; male; pathogenesis; priority journal; scoring system; stem cell; vascular endothelium; vasodilatation; Aged; C-Reactive Protein; Cell Adhesion; Cells, Cultured; Colony-Forming Units Assay; Coronary Disease; Dose-Response Relationship, Drug; Endothelial Cells; Endothelium, Vascular; Exercise; Female; Humans; Male; Microvascular Angina; Middle Aged; Stem Cells; Tumor Necrosis Factor-alpha; Vasodilation [SDGs]SDG3 |
Appears in Collections: | 解剖學暨細胞生物學科所 |
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